4,4 '-Dichlorodiphenyltrichloroethane (DDT) and 4,4 '-dichlorodiphenyldichloroethylene (DDE) promote adipogenesis in 3T3-L1 adipocyte cell culture

Abstract

4,4'-Dichlorodiphenyltrichloroethane (DDT), a chlorinated hydrocarbon insecticide, was extensively used in the 1940s and 1950s. DDT is mainly metabolically converted into 4,4'-dichlorodiphenyldichloroethylene (DDE). Even though most countries banned DDT in the 1970s, due to the highly lipophilic nature and very stable characteristics, DDT and its metabolites are present ubiquitously in the environment, including food. Recently, there are publications on relationships between exposure to insecticides, including DDT and DDE, and weight gain and altered glucose homeostasis. However, there are limited reports regarding DDT or DDE and adipogenesis, thus we investigated effects of DDT and DDE on adipogenesis using 3T3-L1 adipocytes. Treatment of DDT or DDE resulted in increased lipid accumulation accompanied by increased expression of CCAAT/enhancer-binding protein alpha (C/EBP alpha), peroxisome-proliferator activated receptor-gamma (PPAR-gamma), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), adipose triglyceride lipase, and leptin. Moreover, treatment of DDT or DDE increased protein levels of C/EBP alpha, PPAR gamma, AMP-activated protein kinase-ce (AMPK alpha), and ACC, while significant decrease of phosphorylated forms of AMPK alpha and ACC were observed. These finding suggest that increased lipid accumulation caused by DDT and DDE may mediate AMPK alpha pathway in 3T3-L1 adipocytes. (C) 2016 Elsevier Inc. All rights reserved.